Method and apparatus for the treatment of focal dystonia

ABSTRACT

A method and apparatus for using low levels of electrical stimulation to treat focal dystonia by stimulating the afferent nervous system and/or altering the function of the gamma motor neurons innervating muscles which experience symptomatic spasms.

CROSS-REFERENCE TO RELATED APPLICATIONS

This application is a Continuation of U.S. application Ser. No.13/854,031, filed Mar. 29, 2013, entitled “METHOD AND APPARATUS FOR THETREATMENT OF SPASMODIC DYSPHONIA,” which in turn claimed priority toU.S. Provisional Patent Application No. 61/617,537, entitled “METHOD ANDAPPARATUS FOR THE TREATMENT OF SPASMODIC DYSPHONIA” filed on Mar. 29,2012, both of which are hereby incorporated by reference in theirentirety for all purposes.

TECHNICAL FIELD

The present disclosure relates to methods and apparatus for thetreatment of focal dystonia.

BACKGROUND

Focal dystonias are neurological movement disorders characterized byinvoluntary muscle contractions causing spasms, twisting, repetitivemovements, or abnormal postures. Focal dystonias include cervicaldystonia, blepharospasm, focal hand dystonia, and spasmodic dysphonia.These disorders can significantly impact quality of life.

Treatment of dystonia has focused on inhibiting the action of alphamotor neurons which cause the muscles to contract in spasm. For example,historically treatment of spasmodic dysphonia has been aimed atparalyzing or weakening one of the vocal folds in order to decrease itsability spasm and interrupt phonation. Dedo first proposed andpopularized recurrent laryngeal nerve resection as a treatment forspasmodic dysphonia. This was the first and only surgical procedurewhich achieved widespread use. Some surgeons did not want to completelytransect the RLN, and instead crushed it to weaken or paralyze the vocalfolds but keep the nerve intact. Unfortunately, over the long term, themajority of patients who underwent either resection or crush experienceda return of their phonatory spasms. Due to this, both procedures wereeventually abandoned.

Botulism toxin (BTX) injection is a common and “gold standard” treatmentof dystonia. BTX inhibits neural function, and it is thought that itcontrols the symptoms of dystonia by preventing the firing of overactivemotor neurons.

A few researchers have attempted to use electrical nerve stimulation totreat the symptoms of dystonia. Bidus, et al explored the use ofelectrical nerve stimulation to treat abductor spasmodic dysphonia bystimulating the motor nerves to the adductor muscle, causing anantagonistic muscle contraction designed to counteract the spasms causedby the disorder.

Tinazzi et al attempted to use low frequency transcutaneous electricalnerve stimulation (TENS) to treat spasms associated with writers' cramp.TENS was delivered to forearm flexor muscles of ten individualssuffering from writers' cramp at a level of stimulation that was belowthe threshold to cause muscular contractions. The researchers concludedthat the TENS treatment may have therapeutic effects on writers' crampdystonia that lasts for several weeks. The researchers attributed thistherapeutic effect to a reshaping of reciprocal excitatory andinhibitory functions between agonist and antagonist muscles, observingthat those functions are typically severely impaired in dystonia.Specific muscles were not targeted in this therapy, both because theresearchers intended to restore the relationship between agonist andantagonist muscles, which teaches away from the specific targeting ofmuscles, and because the use of TENS made specific targeting impossible.

Apart from these efforts, the use of electrical nerve stimulation hasbeen primarily used to reanimate paralyzed muscle, not to treatspasmodic disorders such as focal dystonia.

BRIEF DESCRIPTION OF THE DRAWINGS

FIG. 1 shows a top view of the larynx.

FIG. 2 is a flow chart illustrating the direction of impulsescommunicated between the central nervous system, the motor neurons, themuscles, the afferent nerves, and the gamma neurons and the impact ofstimulation on gamma motor neurons.

FIG. 3 is a flow chart illustrating the direction of impulsescommunicated between the central nervous system, the motor neurons, themuscles, the afferent nerves, and the gamma neurons and the impact ofstimulation on the afferent system.

FIG. 4 is a cut away view of a muscle spindle.

FIG. 5 is a muscle view of a muscle spindle.

DETAILED DESCRIPTION OF DISCLOSED EMBODIMENTS

As discussed above, the general belief is that symptoms of focaldystonia result from abnormal motor signals to motor neurons whichcontrol the muscles. Abnormal motor neural activity causes muscles tospasm, resulting in the symptoms of focal dystonia. Within this paradigmit is assumed that BTX is effective because it interferes with the motornerves innervating the muscle into which it has been injected, and thusinterferes with the muscle's ability to spasm. The central nervoussystem continues to send abnormal motor signals to motor neurons, butthey are unable to cause muscle contractions as forcefully.

The inventor has realized that contrary to conventional thinking, focaldystonias are more likely caused by abnormal afferent nerve signals andnot abnormal motor nerve signals.

Efferent nerves, also known as motor neurons, carry nerve impulses fromthe central nervous system to effectors such as muscles. They areinvolved in muscular control. Afferent neurons, also known as receptorneurons, carry nerve impulses to the central nervous system. Signalscarried by afferent nerves create sensations that the brain thenidentifies as pain, itch, stretch, etc.

As shown in FIGS. 4 and 5, muscle spindles 10 consist of both gammamotor neurons and afferent (sensory) neurons and are an importantcomponent of muscular proprioception. The intrafusal muscle fibers 12,are innervated by type Ia 16 and type II 18 sensory afferent neurons.They lie parallel to the extrafusal muscle fibers and are innervatedwith afferent nerves which sense muscle length and rate of changes inmuscle length. The gamma motor neuron 14 also innervates the intrafusalfibers 12 of the muscle spindle 10. By causing contraction of theintrafusal muscle fibers, the gamma motor neuron increases thesensitivity of the afferent neurons of the muscle spindle. When alphaneurons fire and cause the muscles to contract the muscle spindlesshorten and become slack, and lose their ability to detect musclelength. To prevent this, when the central nervous system sends signalsvia alpha neurons, co-activating signals are also sent to the gammamotor neurons 14. The gamma motor neurons maintain tautness of musclespindles even as a muscle contracts, and permit the muscle spindles todetect muscle length. Gamma neuron activity is further modulated byinput form the type Ia and type II afferent nerves as they sense changesin muscle length. Thus, the gamma neurons set the sensitivity of musclespindles.

The consistent level of gamma activity is called gamma bias. Overactivegamma neurons with a high bias result in hyper-sensitivity of theafferent nerves of the muscle spindle. As a result, muscle contractionsare inappropriately increased, resulting in a muscle spasm.

Smaller neurons require a smaller amount of stimulation to reach theirexcitability thresholds than larger neurons do, and gamma neurons aresmaller than alpha neurons. As a result, gamma neurons may fire inresponse to a given stimulus where alpha neurons subjected to the samestimulus do not.

As discussed above, it is believed that the symptoms of spasmodicdysphonia result from abnormal motor signals from motor neurons whichcontrol the muscles the larynx. Abnormal motor neuron activity causesthe muscles to spasm, resulting in SD. This understanding of SD has ledto treatments which seek to denervate the larynx, surgically orchemically. It is believed that BTX is effective because it weakens themuscle into which it is injected, and that the weakening effectinterferes with the muscle's ability to spasm. The muscles continue toreceive abnormal motor signals from their innervating motor neurons, butthey are able to respond less forcefully.

However, the inventor has realized that, contrary to the conventionalthinking, spasmodic dysphonia may be caused by abnormal afferent nervesignals and not abnormal motor signals. Abnormal afferent nerve signalswhich originate in the larynx cause abnormal motor signals which in turncause the muscles to spasm. BTX inhibits the function of motor nerves bypreventing nerves from releasing acetycholine at the synaptic junction.BTX may work on the gamma motor neurons in the muscle spindle in muchthe same way as it works on the alpha motor neurons, in that itdecreases activity of both types of nerves via the same mechanism.

Neuromuscular stimulation, on the other hand, is often used to increaseneurologic activity, in other words, cause muscles to contract, e.g., inorder to treat paralysis or paresis. The use of neuromuscularstimulation to impact the afferent nervous system is different in bothobjects and methodology. For example, it is well accepted that theapplication of electrical stimulation to a muscle will cause that muscleto contract when the stimulation rises above the excitability thresholdof the innervating motor neurons. However, the effects of stimulation onthe afferent system are less predictable. Tinazzi, et. al observed thathigh frequency stimulation of peripheral cutaneous nerves for tenminutes in normal subjects produced a decrease in sensorimotor cortexexcitability lasting about 60 minutes, but low frequency stimulation (10Hz) of peripheral nerves of normal subjects for 2 hours produced anincrease in sensorimotor cortex excitability lasting 30 to 40 minutes.To the inventor's knowledge, no one has observed a mechanism wherebyelectrical stimulation is used to lower the activity of motor neuronsthrough the stimulation of the sensory system.

The inventor has realized that subjecting a muscle to a low level ofelectrical stimulation functions as a sensory trick, acting on theafferent nervous system to changing the sensory milieu and interruptingabnormal sensory signaling to the brain, in turn alleviating spasmodicsymptoms. Sensory tricks tend to lose their effectiveness over time.However, the parameters of electrical stimulation can be altereddynamically, and therefore it can better maintain its effectiveness.

The inventor has also realized that a relatively low level of electricalstimulation can alter the gamma loop, reducing the sensitivity ofafferent nerves of the muscle spindle and causing a reduction inabnormal sensory signaling. As shown in FIG. 2, the central nervoussystem 30 sends impulses to alpha motor neurons 32, which act onextrafusal muscles fibers 34. The central nervous system simultaneouslysends impulses to the gamma motor neurons 36, which act on theintrafusal muscle fibers 38 of the muscle spindles. The gamma motorneurons 36 are coactivated with the alpha motor neurons 34 to maintainan appropriate level of sensitivity in the muscle spindle sensoryafferent nerves. The intrafusal muscle fibers act on the afferent nerves39 in the muscle spindles. The afferent nerves 39 send impulses to thecentral nervous system, and possibly the alpha motor neurons 30 and thegamma motor neurons 36. Electrical stimulation 40 of the gamma motorneurons 36 changes how the gamma motor neurons 36 act on the intrafusalfibers 38 and hence alters the sensitivity of the afferent neurons.Inhibiting the gamma neuron 36 via electrical stimulation 40 will resultin a decreased gamma motor neuron bias and will reset the muscle spindlesensory afferent neurons to a lower sensitivity. The high gain of thesystem will be decreased, and when an alpha motor neuron sends a signalfor the extrafusal muscle fibers to contract, the system will no longerbe hypersensitized, and the motor neuron signal will result in anappropriate contraction, not an uncontrolled spasm. Thus, a low level ofelectrical stimulation can provide a means of decreasing gamma motorneuron bias, thus utilizing electrical stimulation to decrease alphamotor neural activity and reduce spasm.

The inventor has also discovered that electrical stimulation can alterthe gamma motor loop by stimulating the afferent neurons, thus utilizingafferent nerve stimulation to alter abnormal alpha motor neuron activityto effectively reduce muscle spasm, as shown in FIG. 3. The centralnervous system 50 sends impulses to alpha motor neurons 52, which fire,causing extrafusal muscle fibers 54 to contract. The central nervoussystem simultaneously sends impulses to the gamma motor neurons 56,which act on the intrafusal muscle fibers 58 of the muscle spindles.This coactivation of the gamma motor neurons and the alpha motor neurons54 maintain an appropriate level of sensitivity in the sensory afferentneurons of the muscle spindle. The intrafusal fibers act on the afferentnerves 59 innervating the intrafusal fibers 58 of the muscle spindle,which may send signals to the gamma and alpha motor neurons and thecentral nervous system 50. Stimulation of the afferent nervesinnervating the intrafusal fibers 58 in the muscle spindles may directlyalter the afferent-efferent loop, decreasing muscle spasm.

Low level, or afferent stimulation, as disclosed herein involvessubjecting a muscle to an electrical impulse delivered by an electrodeplaced near, in contact with, or within the muscle. The stimulatingelectrical impulse may vary by parameter such as duration, amplitude,frequency, and/or duty cycle. These parameters are set and governedusing a processor which is operably connected with one or moreelectrodes which are used to administer the stimulating electricalimpulse. The duty cycle is the duration of time in which an impulse isbeing delivered relative to the duration of time in which no impulse isbeing delivered. An interrupted, or non-continuous pattern ofstimulation alternates periods of delivery of an impulse with periods inwhich no impulse is being delivered. The duty cycle can be variedautomatically by the processor. Additionally, the patient or individualdirecting treatment may turn the stimulator on or off as needed,resulting in an additional source of variation of stimulation.

This stimulating electrical impulse should preferably be delivered tothe specific muscles that undergo symptomatic contraction, and effectsto other structures should be minimized. The electrode or electrodesused to provide stimulation should be associated with or placed incommunication directly with a muscle to be stimulated in a manner thatlimits its impact substantially to that muscle. This can beaccomplished, for example, by placing electrodes in direct contact withthe muscles which experience symptomatic spasm, for example thethyroartenoid (TA) 2, lateral cricoarytenoid 4, interarytenoid orposterior cricoarytenoid 6 muscles in spasmodic dysphonia, as shown inFIG. 1. This placement prevents unspecific stimulation of adjacentstructures, and thereby prevents alteration of normally functioningsensory pathways in adjacent structures.

To treat dystonia, the active end of the stimulator should be placed incommunication with or within the affected muscle and used to provide astimulating signal or impulse at an amplitude and/or frequency that isbelow the excitation threshold of the alpha motor nerves innervating themuscle, and thus too low to cause firing of alpha nerves innervating themuscle fibers, and too low to cause muscle contractions. Thisstimulating electrical signal is sensed by the afferent nerves, causinginterruption of the abnormal afferent-efferent loop that results inlaryngeal spasms and the symptoms of dystonia. Additionally oralternatively, the signal impacts the function of the gamma loop,resetting gamma bias, and desensitizing the muscle spindle, resulting inless excitability and less responsiveness to muscle contractions andother stimuli. The muscle spindle's abnormal afferent signaling will bereduced or eliminated, resulting in normal signals to the alpha motorneurons which will result in normal phonation and instead of vocalspasms.

The electrical stimulation can be produced by a commercially availableneurostimulator using electrodes that are inserted into the muscle mostaffected by dystonia using thin hypodermic needles. The level ofstimulation delivered should be directed to the afferent nerves and thegamma motor neuron, and should be sufficiently weak that it does notproduce muscle contractions by stimulating alpha motor neurons. Signalsthat are too weak to stimulate alpha motor neurons can nonethelessstimulate the afferent nerves of the muscle spindle and/or disrupt theaction of the gamma neuron, changing the sensory nerve activity andgamma bias, preventing spasms of the laryngeal muscles.

The inventor has confirmed this hypothesis by showing that thislow-level neural stimulation applied to the TA muscle is effective intreating spasmodic dysphonia (SD). The inventor has conducted a study todetermine the influence of on-target TA electric stimulation which hasshown that it is safe and effectively relieves the symptoms of SD. Incomparison with TENS stimulation or even with the BTX injection thistype of stimulation will be more precise and will allow betterfine-tuning depending on the individual characteristics and symptomgrade of each patient.

Additionally, on-target TA stimulation prevents the unwanted response ofthe PCA muscle, responsible for vocal cord abduction or the unspecificstimulation of the CT muscles. In this respect, evaluation of theexclusive stimulation of the TA prevents biases and/or artifacts due tothe unspecific stimulation of the contiguous muscles (i.e. PCA and CT).

The innovative treatment represents an on-target treatment for dystonia,thus it is expected to minimize the problems observed in othertherapeutic methods due to their aspecificity. Additionally, astimulator will allow better fine-tuning based on the individual needsof each patient and may become a sound alternative to the presentsymptom-relieving therapies in use for dystonia. Finally, while BTXrequires repeat treatment with painful injections approximately everythree months, the methods disclosed herein require the implantation of astimulation device and no further invasive treatment. The dystonia canbe essentially cured.

A first-in-human, one-arm, cross-over, exploratory, open-label,prospective, longitudinal and monocentric study has confirmed the safetyand efficacy of this treatment as compared to the current gold standardfor the treatment of SD (i.e. BTX injection) within the same patient,thus avoiding the occurrence of biases due to the so called“patient-specific effects”. This is particular important in anobservatory study in which individual characteristics may significantlyaffect the outcome and the total number of patients expected to complywith the selection criteria is low (currently a niche population). Thewash-out period was 12 to 13 weeks. The introduction of the wash-outperiod was designed to minimize biases during the data analysis, due tooverlapping effects between the two treatments.

At the BTX injection visit, patients' medical histories were reviewed,any necessary medical examinations and laryngovideostroboscopy wasperformed. Additionally, patents were taped reading the sentencesconstructed to stimulate vocal spasms (before and at multiple timeperiods after the BTX injection). Patients were also asked to fill out aVoice handicap index-10 and study-specific 5 point liked scale atsimilar time points. Laryngeal Electromyography (LEMG) is a medicalprocedure that records the electrical activity produced by laryngealmuscles in action. During LEMG, electrical activity is recorded,amplified, and displayed on a screen and played on a loudspeaker toallow visual and sound analysis. Specifically in this study, LEMG willbe used to localize the TA for intramuscular injection of botulinumtoxin and placement of the electrical stimulator.

During injection with BTX, the subject was asked to assume a comfortableposition with slightly extended neck. The investigator inserted theneedle electrode into the TA. The subject was then asked to phonate bysaying /i/. Position of the needle tip was confirmed by sharp electricalactivity upon sustained /i/ phonation. Once the needle tip was confirmedto be within the TA the botulinum toxin was injected.

The laryngvideostroboscopy served to record the natural status of thevocal folds as well as vocal fold motion and mucosal wave duringphonation of /i/ at the normal speech frequency.

The on-target TA-specific electrical stimulation was delivered using acommercially available device (CareFusion SYNERGY N series 2 channel EMG& stimulation). The unit is a dual-channel bipolar device that suppliesmonophasic pulsed current.

Since regular needle electrodes do not consistently maintain theirintra-muscular position over the course of 20 to 60 minutes due tomovement of related tissue, hooked-wire electrodes were used. Thisdecision was also made due to the reduced size of the TA muscle and itsrelatively high inaccessibility that make the use of surface electrodesunfeasible. Hooked-wire electrodes were made by passing 1 or 2 very thinwires through a hypodermic needle. The end of the wire at the tip of theneedle was bent down to form a “hook”. The needle was inserted into themuscle and pulled out so that the wire hooked around the muscle fibers,securely held in position.

Placement for the hook wire electrodes was into the thyroarytenoidmuscle.

Position of the hooked electrodes was verified using recognized adductortasks: increased muscle activity during prolonged phonation of /i/vowels and a valsava. The stimulation was delivered according to thefollowing parameters:

1) Frequency: nominal 50 Hz (range 20-200 Hz)

2) Impulse duration: nominal 200 (range 50-750) microseconds

3) Impulse amplitude: is set below pain threshold and is too low tocause muscular contraction, range from 0 to 3 mA (tolerance±10%)

4) Stimulation treatment duration: 60 minutes

5) Simultaneous laryngoscopy confirmed an absence of stimulation inducedmuscle contraction.

The stimulation was repeated five times on five consecutive days. Beforeand after each stimulation session subjects' answers to the likert scaleand evaluation of taped readings of sentences constructed to stimulatevocal spasms showed that patients and trained listeners perceivedimproved voice quality compared to the baseline. After the 5 sessions ofstimulation a Voice handicap index-10 was also completed by thepatients, again showing decrease of their vocal handicap over the week.Carry over of vocal improvement lasted days to weeks and was rated againwith a liked scale, taped reading and the Voice handicap index-10 atsimilar time periods as was performed after BTX injection. Improvementin symptoms indicated that a low level of electrical stimulation, toolow to affect the alpha motor nerves, resulted in decreased vocalspasms, improvement in voice comparable to BTX injections and confirmedthe efficacy of the stimulation mechanism described herein.

Stimulation delivered in accordance with the inventions disclosed hereinshould preferably be delivered in a varied pattern over time rather thanin a continuous manner. Parameters such as frequency, amplitude, andduty cycle which are inherently governed by the processor or by patientmanipulation of the processor duty cycle, should be varied. Patients mayturn the stimulator on or off as needed for treatment.

It is suspected that the sensory nervous system and the central nervoussystem, will acclimate to a given level of constant stimulation andcause the stimulation to lose its effectiveness over time. Variation inthe frequency, amplitude or duty cycle of the stimulating electricalimpulse should be used to avoid acclimation.

The terms and expressions which have been used in this specification areintended to describe the invention, not limit it. The scope of theinvention is defined and limited only by the following claims.

What is claimed is:
 1. A method of treating focal dystonia comprising:a. providing a system comprising a stimulating electrode operablyconnected with a processor configured to set one or more stimulationparameters for an electrical impulse deliverable by the electrode; b.placing the electrode in contact with at least one neuron innervating atleast one muscle; c. using the processor to set the stimulationparameters such that the electrical impulse causes a level ofstimulation which does not exceed an excitability threshold of one ormore alpha motor neurons located within the at least one muscle; and d.delivering the electrical impulse to the at least one neuron, whereinthe electrical impulse acts upon one or more muscle spindles locatedwithin the at least one muscle.
 2. The method of claim 1, wherein theelectrical impulse has an amplitude, a frequency, and a duty cyclegoverned by the processor, and wherein at least one of the amplitude andthe frequency and the duty cycle are varied during treatment.
 3. Themethod of claim 1, wherein the electrical impulse acts upon one or moregamma motor neurons located within the at least one muscle.
 4. Themethod of claim 3, wherein the stimulating electrical impulse decreasesthe level of activity of the one or more gamma motor neurons.
 5. Themethod of claim 1, wherein the electrical impulse acts upon one or moreafferent neurons located within the at least one muscle.
 6. The methodof claim 5, wherein the stimulating electrical impulse decreases thelevel of activity of the one or more afferent neurons.
 7. The method ofclaim 5, wherein the stimulating electrical impulse inhibits at leastone neural signal transmitted to a central nervous system by the one ormore afferent neurons.
 8. A method of treating focal dystonia comprisingusing an electrode in communication with a processor to deliver anelectrical impulse to at least one neuron innervating at least onemuscle, wherein the impulse delivers a level of stimulation that isbelow an excitability threshold of alpha motor neurons innervating theat least one muscle, and wherein the electrical impulse acts upon agamma loop.
 9. The method of claim 8, wherein the electrical impulse hasan amplitude, a frequency, and a duty cycle governed by parameters setby the processor, and wherein at least one of the amplitude and thefrequency and the duty cycle are varied during treatment.
 10. The methodof claim 8, wherein the electrical impulse acts upon one or more gammaneurons located within the at least one muscle.
 11. The method of claim10, wherein the electrical impulse decreases a level of activity of theone or more gamma neurons.
 12. The method of claim 8, wherein theelectrical impulse acts upon one or more afferent neurons located withinthe at least one muscle.
 13. The method of claim 12, wherein thestimulating electrical impulse decreases the level of activity of theone or more afferent neurons.
 14. The method of claim 12, wherein thestimulating electrical impulse alters or inhibits at least one neuralsignal transmitted to a central nervous system by the one or moreafferent neurons.
 15. A system for treating focal dystonia comprising anelectrode configured to deliver an electrical impulse to at least oneneuron innervating at least one muscle, the electrode being incommunication with a processor configured to set one or more stimulationparameters governing the electrical impulse, wherein the processorcauses the electrical impulse to deliver a level of stimulation to theat least one neuron, the level of stimulation being below anexcitability threshold of alpha neurons innervating the muscle, andwherein the electrical impulse acts upon one or more afferent neurons.16. The system of claim 15, wherein the electrical impulse has anamplitude, a frequency, and a duty cycle governed by the one or morestimulation parameters, and wherein at least one of the amplitude andthe frequency and the duty cycle are varied during treatment.
 17. Thesystem of claim 15, wherein the electrical impulse acts upon one or moregamma neurons located within the at least one muscle.
 18. The system ofclaim 17, wherein the electrical impulse decreases a level of activityof the one or more gamma neurons.
 19. The system of claim 15, whereinthe electrical impulse decreases a level of activity of the one or moreafferent neurons.
 20. The method of claim 15, wherein the electricalimpulse inhibits at least one neural signal transmitted to a centralnervous system by the one or more afferent neurons.
 21. A method oftreating focal dystonia comprising: a. providing a system comprising astimulating electrode operably connected with a processor configured toset one or more stimulation parameters for an electrical impulsedeliverable by the electrode; b. placing the electrode in contact withat least one neuron innervating at least one muscle; c. using theprocessor to set the one or more stimulation parameters such that theelectrical impulse causes a level of stimulation that does not exceed anexcitability threshold of one or more alpha motor neurons located withinthe at least one muscle; and d. delivering the electrical impulse to theat least one neuron, wherein the electrical impulse acts upon a gammaloop.
 22. The method of claim 21, wherein the electrical impulse actsupon one or more gamma motor neurons located within the gamma loop. 23.The method of claim 21, wherein the electrical impulse acts upon one ormore afferent neurons located within the gamma loop.
 24. A method oftreating focal dystonia comprising using an electrode in communicationwith a processor to deliver an electrical impulse to at least one neuroninnervating at least one muscle, wherein the impulse delivers a level ofstimulation that is below an excitability threshold of alpha motorneurons innervating the at least one muscle, and wherein the electricalimpulse acts upon a gamma loop.
 25. The method of claim 24, wherein theelectrical impulse acts on one or more gamma neurons located within thegamma loop.
 26. The method of claim 24, wherein the electrical impulseacts upon one or more afferent neurons located within the gamma loop.27. A method of treating focal dystonia comprising: a. providing asystem comprising a stimulating electrode operably connected with aprocessor configured to set one or more stimulation parameters for anelectrical impulse deliverable by the electrode; b. placing theelectrode in contact with at least one neuron innervating at least onemuscle; c. delivering the electrical impulse to the at least one neuron,wherein the electrical impulse acts upon one or more afferent neuronslocated within the at least one muscle.
 28. A system for treating focaldystonia comprising an electrode configured to deliver an electricalimpulse to at least one neuron innervating at least one muscle, theelectrode being in communication with a processor configured to set oneor more stimulation parameters governing the electrical impulse, whereinthe processor causes the electrical impulse to deliver a level ofstimulation to a neuron placed in communication with the electrode, thelevel of stimulation being below an excitability threshold of alphaneurons innervating the at least one muscle, wherein the electricalimpulse acts upon a gamma loop.
 29. The system of claim 28, wherein theelectrical impulse acts upon one or more gamma neurons located withinthe gamma loop.
 30. The method of claim 29, wherein the electricalimpulse acts upon one or more afferent neurons located within the gammaloop.